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CPR Exam 1 > Chapter 14 > Flashcards

Chapter 14 Flashcards

1
Q

What is the final common result of ischemia medial damage and marfans that can lead to the formation of an aneurism?

A

Cystic medial degeneration

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2
Q

Abdominal aortic aneurisms are characterized by severe atherosclerosis of the aorta, and are frequently covered by what?

How can we detect?

A
  • Mural thrombus
  • Pulsating mass in the abdomen
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3
Q

Aortic dissections occur when blood enters a defect in the intima and travels though the tissure between the aortic media. Who do aortic dissection most commonly occur in?

A
  • 1. HTN males 40-60 YO
    1. Pts with CT disorders (Marfan)
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4
Q

What is the main risk factor in a aortic dissection?

A

HYPERTENSION

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5
Q

How does a patient with an aortic dissection present?

A

Sudden onset of severe CP that radiates to the back between the scapula and moves downward as the disscection progresses.

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6
Q

What is most commonly confused with a acute MI?

A

Aortic dissection

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7
Q

Who are AAA more common in?

A

Men

Smokers

60s

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8
Q

Thoracic aortic aneurism are most often due to what?

A
    1. HTN
    1. Marfans: Defective fibrillin and overactive TGF-B, which weakens elastic tissue
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9
Q

Note that we often see __________ in pts with aortic dissections.

A

cystic medial degeneration

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10
Q
  • Large vessel vasculitis includes aorta and branches (2)
A
  • Temporal (Giant cell) arteritis
  • Takayasu arteritis
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11
Q
  • Med vessel vasculitis affects muscular arteries, which supply organs
A
  1. Polyarteritis nodosa (PAN)
  2. Kawasaki disease
  3. Buerger disease
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12
Q
  • Small vessel vasculitis affects arterioles, capillaries and venules.
A
  1. Wegener granulomatosis
  2. Microscopic polyangiitis
  3. Churg-Strauss syndrome
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13
Q

Notice that __________ is the only vasculitis that involves the aorta.

A

giant cell arteritis

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14
Q

_______ requires eosinophils and is associated with asthma and atopic individuals.

A

Churg-Strauss

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15
Q

________ requires neutrophils and is associated with orogenital ulcers.

A

Behçet disease

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16
Q

_________ is associated with young male smokers.

A

Buerger disease

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17
Q

If we see a patient and ID immune complexes in the vascular wall, what do we do?

A

Assume DRUG HYPERSENSITIVITY!

Stop the drug => vasculitis should resolve.

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18
Q

Antineutrophil cytoplasmic antibodies (ANCA) are what?

A

autoAB against enzymes inside of cytoplasm of neutrophils, monoxytes and endothelial cells.

ANCA bind to neutrophils => activate them => cause the release of ROS and cytokines => inflame and damage endothelium => vasculitis

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19
Q

Do vasculitis assx with ANCA have immune complexes?

A

NO. ANCA produces a pausi-immune response => attack things inside of neutrophils but do not form immune comples. THUS THESE LESIONS WILL NOT HAVE IMMUNE COMPLEX DEPOSITS

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20
Q

PR3-ANCA/c-ANCA) target PR3 and is assx with what vasculitis?

A

Wegners

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21
Q

Anti-MPO/p-ANCA is asociated with what vasculitis?

A

1. Microscopic polyangiitis

2. Churg-Strauss

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22
Q

Measuring ANCA can tell us

A

how serious the disease is.

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23
Q

Immune complex vasculitis is seen in

A
  1. Lupus
  2. Drug hypersensitivity
  3. Secondary to exposure to infection (Hep B => Polyarteritis nodosa)
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24
Q

_________ are the most common causes of aortitis…

A

Giant Cell Arteritis and Takayasu

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25
Q

Non-infectious vasculitis occur how?

A

Immune-mediated

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26
Q

In what vasculitis does fibrinoid necrosis occur?

A

Small-cell vasculitis

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27
Q
  • Most common form of vasculitis in older patients (>50 YO); F
A

Giant cell arteritis

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28
Q

Giant cell arteritis stems from an immune response by which cells and causes inflammation of arteries where?

A
  • CD4+
  • Proximal aorta, carotid artery and branches
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29
Q

Histo in Giant cell arteritis

A
  • CD4+ cells are going to infiltrate the internal elastic lamina and the media.
  • MO invate the media and form multinucleated giant cells inside of a granuloma.
  • Fragmented ILA and intimal thickening => narrow lumen and ischemia
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30
Q

Inflammation in Giant cell arteritis is what?

A

Patchy and segmental

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31
Q

Sx in giant cell arteritis

A
    1. Temporal artery: HA, facial pain on temporal area
    1. JAw claudication
    1. Opthalmic artery: visual disturbacne and double vision
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32
Q

Takayasu arteritis most commonly affects who

A

Japanese (AZN) females under 40.

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33
Q

Takayasu Arteritis (aka pulseless disease)

A

Granuloma vasculitis of medium and large arteries characterized by ocular disturbances and marked weak pulses/ low BP in the UE’s

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34
Q

Takayasu arteritis has similar histological findings as those seen in giant cell arteritis (T-cells infiltrate of media and intimal elastic lamina, granulomas and intimal thickening, patchy and focal), except involves which vessels?

A

Medium and large vessels: Aortic arch and nearby (pulmonary (1/2), carotid and renal); NOT TEMPORAL

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35
Q

Since many features of Takayasu arteritis are shared with Giant Cell arteritis, the distinction between the 2 is primarily made how?

A
  • AGE of the pt
  • Takayasu = younger(<50 yo)
  • Giant cell = older (>50 yo)
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36
Q

Sx in Takayasi

A
  • Initial sx are non-specific (fatigue, WL, fever, etc)
  • Later
    • Vascular symptoms: “pulseless disease” because the lumen of brachiocephalic / carotid / subclavian arteries narrows => decrease BP => weak/absent UE/carotid pulses
      • Bruits form d/t turbulent blood flow
    • Vascular symptoms then go down to the abdominal aorta and distal aorta
      • Pulmonary HTN
      • MI
      • Renal HTN
      • Limb claudication (pain w walking that is relieved w rest
    • Ocular disturbances: visual disturbances, retinal hemorrhage, blindness

.

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37
Q

Polyarteritis Nodosa (PAN) is what

A

fibrinoid necrosis that involves multiple medium sized arteries and involves many organs (SPEC RENAL), but NOT the lungs (pulmonary vessels).

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38
Q

PAN most commonly affects the _____, but not the _____

A

MC: KIDNEYS

NOT: lungs

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39
Q

In 1/3 of pt’s with polyarteritis nodosa the vasculitis is attributable to chronic infection by which virus?

Immune-complexes composed of what?

A

HBsAg and anti-HBsAg = Chronic HBV

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40
Q

What process does PAN cause vasculitis

A

most likely immune complex mediated

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41
Q

List the 4 vessels most often involved in Polyarteritis Nodosa in descending order of frequency.

A
  1. - Kidneys
  2. - Heart
  3. - Liver
  4. - GI tract
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42
Q

Histo of PAN

A
  • Polyarteritis nodosa results in a beads on a string appearance that are not circumferential. Because PAN causes acute flares and relapses , it makes lesions at varying stages.
    • Early lesions are segmental, transmural (occur across the entire wall= PAN) necrotizing inflammation at BRANCH POINTS (NO GRANULOMAS)
      • Often time we can see immune complexes in wall of BV.
    • As the wall weakens, they can create an aneurism.
    • Lesions that heal => fibrosis, creating the beads on a string.
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43
Q

In PAN are sites of inflammation circumferential

A

NO

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44
Q

Classic Polyarteritis Nodosa is characterized by what morphological pattern of inflammation?

A

Segmental TRANMURALnecrotizing inflammation of small- to medium-sized arteries that can heal and fibrose

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45
Q

During acute phase of Polyarteritis Nodosa the transmural inflammation of arterial wall shows a mixed inflammatory infiltrate and is often accompanied by what type of necrosis?

A

Fibrinoid necrosis

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46
Q

Polyarteritis Nodosa is typically a disease affecting which age group?

Typical course of the disease?

A
  • Young
  • Remitting and episodic
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47
Q

Does Polyartertis nodosa form granulomas?

A

NO

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48
Q

What is a “classic” presentation (signs/sx’s) of Polyarteritis Nodosa?

A

1. Rapidly accelerating HTN

2. Abdominal pain and bloody stools

3. Myalgias and peripheral neutitis

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49
Q

Tx of PAN

A

immunosupression; because immune complex mediated

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50
Q

Kawasaki disease

who does it affect

A

Acute arteritis of the coronary arteries (medium) that affect kids and infants under 4

51
Q

Clinical significance of Kawasaki Disease stems from its predilection for which artery?

Leading to what?

A

Coronary artery

Aneurisms => thrombosis or rupture => <strong>MI</strong>

52
Q

What is the morphology of the vasculitis seen in Kawasaki Disease; differs from PAN how?

A

Dense transmural inflammatory infiltrate w/ LESS prominent fibrinoid necrosis than in PAN

53
Q

Kawasaki disease typically presents with what signs/sx’s?

*First Aid Mnemonic

A

CRASH and burn

  • Conjunctival injection
  • Rash (polymorphous -> desquamating)
  • Adenopathy (cervical LN enlargement = mucocutaneous LN syndrome)
  • Strawberry tongue (erythema and blistering of oral mucosa)
  • Hand and feet are red
  • Burn = FEVER for longer than 5 days
54
Q

If Kawaksaki Disease is recognized early in its course treatment with what will sharply reduce the risk of symptomatic coronary artery disease?

A

IV immunoglobulin and Aspirin

55
Q

Microscopic polyangiitis generally affects which type of vessels?

A

Capillaries + small arterioles and venules

56
Q

How do the age and distribution of the lesions seen in Microscopic Polyangiitis differ from PAN?

A

Tend to be of the same age and are distributed more widely

57
Q

Microscopic polyangiitis affects vessels of many organ systems, but which 3 systems are most common?

A
  • -Kidneys (90% have necrotizing glomerulonephritis)
  • -Lungs (pulmonary hemorrhage)
  • -Skin (palpalble pupura
    *
58
Q

What are other names for micrscopic polyangittis

A
  1. Hypersensitivity vasculitis
  2. leukocytoclastic vasculitis
59
Q

MPA can be features of what 3 disorders

A
  1. Henoch-Schonlein purpura
    • Essential mixed cryoglobulinemia
    • Vasculitis assoc. w/ CT disorders
60
Q

What is seen on histo of MPA?

A
  • P-ANCA will be destroying neutrophils (thus, many fragmented PMNs) => cause segmental fibrinoid necrosis
61
Q

Does MPA form granulomas?

A

NO

62
Q

Which immune cells are seen infiltrating in microscopic polyangiitis, many of which are undergoing apoptosis and giving rise to the term leukocytoclastic vasculitis?

A

NEutrophils (Fragment PMN)

63
Q

What are the major clinical features (signs/sx’s) seen with microscopic polyangiitis?

A
  • Hemoptysis (cough up blood)
  • Hematuria and Proteinuria (pee blood/proteins)
  • Bowel pain or bleeding
  • Muscle pain or weakness
  • Palpable cutaneous purpura
64
Q

What vasculitis is a pulmonary-renal syndrome?

A

MPA

65
Q

What does MPA stain + for and and what other vasculitis has palpable purpure

A
  1. p-ANCA
  2. Churgg-Strauss
66
Q

Q: How is MPA different from PAN?

A
  • Small BV; lesions are same age and more widely distributed
67
Q

What is Churgg Straus disease often misdx with?

A

1. Allergies

2. Allergici rhinitis

3. Asthma

CHURGG!

68
Q

What is Churgg Strauss disease?

A

small-vessel necrotizing vasculitis that involves mainly the heart and lungs. !!!

69
Q

Churgg-Strauss syndrome may have inflammation that resembles PAN or microscopic polyangiitis with the addition of what 2 things?

A

1. HIGH AMOUNT OF EOSINOPHILS

2. NECROTIZING GRANULOMAS

70
Q

What is the primary manifestation of Churg-Strauss Syndrome affecting the kidneys?

A

Focal and segmental glomerulosclerosis

71
Q

What is the primary manifestation of Churg-Strauss Syndrome affecting the myocardium?

Clinically significant why?

A

Cardiomyopthy: MCC of death in this

72
Q
  • Cutanous involvement of Churg-Strauss Syndrome presents with what?
A

Palpalpe purpura, also seen in MPA

73
Q

Behçet Disease is a vasculitis that affects small-medium vessels that presents w what triat?1

A

1. Oral ulcers

2. Genital ulcers

3. Uveitis

74
Q

Which HLA haplotype is associated with Behcet Disease?

A

HLA-B51

75
Q

Vessel inflammation in Behcet Disease is due to what inflammatory cell type?

Recruited by which T cells?

A

Neutrophils, recruitsed by TH17 cells

76
Q

Mortality seen in Behcet Disease is related to what 2 complications?

A

1. Neruo involvemtn

2. Rupture of aneurism

77
Q

MPO-ANCA’s (P-ANCA) are found in what 2 types of non-infectious vasculitis?

A
  1. MPA
  2. Churgg Strauss
78
Q

C-ANCA (PR3) is assx with

A

weCners

79
Q

Granulomatosis with Polyangitis (Wegener granulomatosis) is a c-ANCA (PR3-ANCA) + necrotizing vasculitis characterized by a triad of what?

A
  • 1) Necrotizing granulomas of upper or lower respiratory tract, or both
    2) Necrotizing or granulomatous vasculitis most prominenetly in lungs
    3) Focal necrotizing, often CRESCENTERIC, glomerulonephritis
80
Q

Granulomatosis with polyangiitis is a form of hypersensitivity mediated by what?

A
  • Inhalation of airborne toxin => T-cell mediated hypersensitivy => develops c-ANCA (PR3-ANCA) =>
81
Q

Which sex is more often affected by granulomatosis with polyangiitis and at what age?

A

men 40 YO

82
Q

What are the classic features (signs/sx’s) of granulomatosis with polyangiitis? (4)

A
    • Persistent pneumonitis w/ bilateral nodular and cavitary infiltrates
  2. - Chronic sinusitis
    • Nasopharyngeal ulcerations
    • Evidence of renal disease
83
Q

How serious is granulomatosis with polyangiitis if left untreated?

A

rapidly; 80% will die

84
Q

which vascilitis has

granulomas with GEOGRAPHIC patterns of central necrosis?

A

WEGNERS (GPA)

85
Q

What may be seen radiographically in the lower respiratory tract of pt w/ granulomatosis with polyangiitis as multiple necrotizing granulomas coalesce?

A

centrally cavitating lesions

86
Q

Which renal lesions may be seen early on in granulomatosis with polyangiitis?

Eventually progress to what in late stages?

A

- Focal and segmental glomerulonephritis

- Crescenteric glomerulonephritis

87
Q

Thromboangiitis Obliterans (Buerger Disease) is STRONGLY assx with tobacco smoke in ppl YOUNGER 35 YO and affects TIBIAL and RADIAL As

  • Israeli, Indian, and Japanese groups who have a hypersensitivity to tobacco products.
  • Segmental thrombosis w/ microabcesses formed => total obliteration of distal vessel lumens => distal ischemia of the of distal extremities
    • Tibial and radial arteries=> loss of the fingers and toes.
    • Inflammation of affected vessels can spread to veins and nerves => neuropathy =>
      • Cold-induced Raynaud phenomenon
      • Intermittent claudication (pain with XRCISE that stops with rest)
      • Superficial phlebitis (venous inflammation)
      • Ulcers and gangrene of fingers and toes.
  • Causes severe pain, even at rest.
  • Histo:
    • Segmental, granuloma formation with thrombus that may have microabsesses that obliterates lumen of vessel.
A
88
Q

Which 3 organisms can directly invade vessels and cause infectious vasculitis?

A

- Pseudomonas

- Aspergillus

- Mucor

89
Q

Infectious vasculitis usually spreads how?

A

· Infection of local tissue, however, they can spread through the blood too.

90
Q

Vascular infections (infective vasculitis) can weaken arterial walls and can result in what clinically significant events?

A

· Mycotic aneurysms or cause thrombosis and infarction

91
Q

What is Raynaud’s phenomenon?

A

Excessive vasospasm (RED, WHITE and BLUE) of small arteries and arterioles, in the fingers and toes: proximal vasodilation, central vasoconstriction and distal cyanosis

92
Q

How does Primary Raynaud’s vs. Secondary differ in their symmetry of involvement of the digits?

A

Primary has symmetrical involvement of the digits and is not associated with an underlying disease. It is caused cold or emotion.

· Most common in young F, benign

  • Secondary has asymmetrical involvement of the digits and is assx with a underlying condition: SLE, scleroderma. Gets worse w time.
93
Q

Excessive vasoconstriction of myocardial arteries or arterioles which may cause ischemia or infarct is known as what?

A

· Cardiac Raynaud

94
Q

What are endogenous and exogenous agnts that can prolonged myocardial vessel contraction?

A
  • Endogenous: EPI or a pheochromacytoma
  • Exogenous: cocaine
95
Q

Cardiac Raynaud can result in what?

A
  1. Sudden cardiac death
  2. takotsubo cardiomyopathy “broken <3” syndrome d/t emotional distress
96
Q

Varicose veins are abnormally dilated, tortous veines caused by prolonged, increased intraluminal pressure and most often affect which veins?

A

Superficial veins or the upper and lower legs.

97
Q

What are complications of varicose veins?

A
  • Stasis
  • congestion,
  • stasis dermatitis (pain and ischemia on overlying skin),
  • poor wound healing,
  • ulcers
98
Q

How frequent do emboli arise from superficial LE veins?

A

RARE, compared to deep LE veins (DVT).

99
Q

What can cause esophageal varices and why are they clinically important?

A
  • Portal HTN: opens shunt and sends blood to veins at GE junction: they can rupture and kill.
100
Q

What are hemorrhoids

A

Dilation of venous plexus at anorectal junction

101
Q

What is thrombophlebitis and where does it most commonly occur?

A

inflammatory process that causes blood clot to form and block a VEIN, usually in your leg (forms DVT)

102
Q

What is the most serious potential complication associated with DVT’s and is often the first manifestation of thrombophlebitis

What are the most important risk factors for developing a DVT?

A
  1. PE
  2. prlong activity/not moving; hypercoagulbility
103
Q

What is migratory thrombophlebitis (Trousseau syndrome)?

MCC in?

A
  • A clot that moves around the body: appears at one site, disappears, then goes to another.
  • Mucin secreting ADENOCARCINOMAS, often a paraneoplastic syndrome
104
Q

What are the major causes of Superior Vena Cava Syndrome?

A

neoplasms

aortic aneurysms

105
Q

What is Superior vena cava syndrome

A

pressure on the SVC is due to a neoplasm compressing it => leads to cyanosis and dilation of the veins of the head, neck and arms and can cause respiratory distress if pulmonary vessels are compressed

106
Q

What is inferior vena cava syndrome

A

neoplasma compress IVC or thrombosis of hepatic, renal or LE veins that go up =>

  1. LE edema,
  2. distension of superficial collateral vein in the lower abdomen.
  3. If the kidneys are involved => massive proteinuria.
107
Q

Which 2 cancers have a tendency to grow within veins and may ultimately lead to inferior vena cava syndrome?

May also be caused by thrombosis from where?

A
  • - Hepatocellular carcinoma
  • - Renal cell carcinoma
  • - Thrombosis of the hepatic, renal, or LE veins which propogate cephalad
108
Q

Most common agent of lymphangitis is

A

Group A B-hemolytic Strep

109
Q

;/hat is lymphangitis and what most commonly causes it?

A
  • acute inflammation and the spread of bacterial infection into the lymphatics => red painful subcutaneous streats and painful enlargement of draining LN
110
Q

What is lymphadenitis

A

painful enlargment of draining LN

111
Q

_______ lymphedema is congenital, either an isolated defect or “familial Milroy disease,” which is lymphatic agenesis

A

Primary

112
Q

____ lymphedema is a blockage of previously normal lymphatics d/y tumor, etx

A

secondary

113
Q

peau d’ orange is an example of what

A

secondary (obstructive lymphedema)

  • Tumor cells block draining lymphatic from breast cancer, causing the skin over it to look like ORANG PEELS
114
Q

local dilation of a structure

A

Ectasia

115
Q

A permanent dilation of a small vessels that forms a red lesion in the skin or mucous membrane. They can be congenital or acquired. What are they called and are they true neoplasms?

A
  • Telangiectasia; no
116
Q

Nevus flammeus

A

: a vascular ectasia that forms a light pink-purple birthmark on the head or neck d/t dilated vessels. They often regress by themselves

117
Q

How do Cavernous Hemangiomas differ in terms of infiltration and regression as compared to Capillary Hemangiomas?

A
  • Are more infiltrative and frequently involve deep structures
  • Do NOT spontaneously regress
  • Locally destructive!
118
Q

_______ are very common tumors characterized by increased numbers of normal or abnormal BV

A

hemangiomas

119
Q

Congenital (juvenile/strawberry) hemangiomas often what…

A

REGRESS

120
Q

What is a capillary hemangioma

A

most common; thin wall capillaries are tightly packed 2gether

121
Q

what is this

A

Cavernous hemangiomas: irregular, dilated BV form a lesion with a irregular border, often involving deep tissue and are more likely to bleed

122
Q

____________ (lobular capillary hemangioma) are actually rapidly-growing hemangiomas that exist the oral mucosa and can ulcerate.

When do they commonly occur?

A

Pyogenic granuloma

Granuloma gravidarium (pregnany tumor:

123
Q

What is a pyogenic granuloma

A

A CAPILLAR HEMANGIOMA!

not a pyogenic granuloma

124
Q
A

CPR Exam 1 (19 decks)

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